Jian Li, Ph.D.

My 101

In my lab, we use cellular and animal models to study the basic mechanisms underlying age-related neurodegeneration and cancer. Though it might not seem like it, these two areas of research are related.

One bridge that connects them at the molecular level is what we call “stress-response factors.” These are a group of transcription factors defined by their function. Their job is to regulate gene expression to cope with stressors, such as high temperatures, infections, and whatever environmental disturbances come our way.

These stress-response factors are well-maintained and have an essential pro-survival role. My lab aims to use the roundworm C. elegans as a model to study how these could be used to mediate health decline in aging and provide potential treatment avenues for age-related diseases, specifically neurodegenerative disorders like the Alzheimer’s, Huntington’s, and Parkinson’s diseases. While strengthening the stress-response pathways and increasing survival is good in that context, there is a flipside to that coin: cancer.

Stress-response factors can be activated and re-purposed in a bad way under certain pathological conditions. One example is malignant transformation in cancer, in which dampening the pro-survival function of stress-response is beneficial. Our lab tries to find the switch for stress-response factors that leads to either health enhancement in aging or supporting malignancy, so that we can kill cancer cells without affecting the normal ones. That is why I study both sides of the coin when it comes to understanding these transcription factors.